Abstract
BackgroundAdipose and hepatic metabolic dysfunctions are critical comorbidities that also aggravate insulin resistance in obese individuals. Melatonin is a low-cost agent and previous studies suggest that its use may promote metabolic health. However, its effects on some comorbidities associated with obesity are unknown. Herein, we investigated the hypothesis that melatonin supplementation would attenuate adipose-hepatic metabolic dysfunction in high fat diet (HFD)-induced obesity in male Wistar rats.Materials and methodsTwenty-four adult male Wistar rats (n = 6/group) were used: Control group received vehicle (normal saline), obese group received 40% high fat diet, melatonin-treated group received 4 mg/kg of melatonin, and obese plus melatonin group received 40% HFD and melatonin. The treatment lasted for 12 weeks.ResultsHFD caused increased food intake, body weight, insulin level, insulin resistance and plasma and liver lipid but decreased adipose lipid. In addition, HFD also increased plasma, adipose and liver malondialdehyde, IL-6, uric acid and decreased Glucose-6-phosphate dehydrogenase, glutathione, nitric oxide and circulating obestatin concentration. However, these deleterious effects except food intake were attenuated when supplemented with melatonin.ConclusionTaken together, the present results indicate that HFD exposure causes adipose-hepatic metabolic disturbance in obese animals, which are accompanied by oxidative stress and inflammation. In addition, the present results suggest that melatonin supplementation attenuates adipose-hepatic metabolic dysfunction, accompanying obesity by suppression of oxidative stress/inflammation-dependent mechanism and increasing circulating obestatin.
Highlights
Obesity has become a global epidemic in the twenty-first century
The present results indicate that high fat diet (HFD) exposure causes adipose-hepatic metabolic disturbance in obese animals, which are accompanied by oxidative stress and inflammation
The data from the present study demonstrated that melatonin reversed the adipose-hepatic metabolic comorbidities associated with obesity in male Wistar rats by suppression of oxidative stress, inflammation and increasing circulating obestatin
Summary
Obesity has become a global epidemic in the twenty-first century. Overweight individuals aged 18 and above accounted for more than 1.9 billion people in 2016. Diverse disease influenced by hormones, nutritional consumption, sedentary lifestyles, physical activity, genetics, and environmental variables [2, 3]. This metabolic disease is rising with comorbidities, including non-alcoholic fatty liver disease (NAFLD) that reduce life quality and expectancy, primarily due to cardiometabolic problems [4]. The pathogenesis of cardiometabolic dysfunctions are low-grade systemic inflammation and insulin resistance caused by cytokines These cytokines are released by excess adipose tissue in the body, especially in the visceral site [5,6,7]. Adipose and hepatic metabolic dysfunctions are critical comorbidities that aggravate insulin resistance in obese individuals. We investigated the hypothesis that melatonin supplementation would attenuate adipose-hepatic metabolic dysfunction in high fat diet (HFD)-induced obesity in male Wistar rats
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